MR arthrography of elbow: evaluation of the ulnar collateral ligament of elbow

 Objective. The purpose of this study was to evaluate ulnar collateral ligament (UCL) injury of the elbow in throwing athletes by MRI and MR arthrography. Design. Ten elbows of throwing athletes were examined on both plain MRI and MR saline arthrography and the injuries subsequently surgically proven. Spin-echo (SE) T1-weighted and fast SE T2-weighted coronal images were obtained. Results. The UCL was unclear in all ten cases on T1-weighted MRI. In five cases an avulsion fracture was also found on T1-weighted MRI. On T2-weighted MRI, abnormal high-intensity areas were identified in or around the UCL. On T2-weighted MR arthrography images, extracapsular high-intensity areas, which represent extracapsular leakage, were found in four of five cases with avulsion fracture. At surgery, all these four cases showed avulsion fractures with instability; the other case had a fracture but it was stable and adherent to the humerus. On T2-weighted MR arthrography images, an extracapsular high-intensity area was found in one of the five cases without avulsion fracture. At surgery this patient had a complete tear of the UCL itself. Conclusion. MR arthrography provided additional information for evaluating the degree of UCL injury.     

Characterization of the Amino Acid Transport of New Immortalized Choroid Plexus Epithelial Cell Lines: A Novel In Vitro System for Investigating Transport Functions at the Blood-Cerebrospinal Fluid Barrier

Purpose. To establish and characterize a choroid plexus epithelial cell line (TR-CSFB) from a new type of transgenic rat harboring the temperature-sensitive simian virus 40 (ts SV 40) large T-antigen gene (Tg rat).Methods. Choroid plexus epithelial cells were isolated from the Tg rat and cultured on a collagen-coated dish at 37°C during the first period of 3 days. Cells were subsequently cultured at 33°C to activate large T-antigen. At the third passage, cells were cloned by colony formation and isolated from other cells using a penicillin cup.Results. Five immortalized cell lines of choroid plexus epithelial cells (TR-CSFB 15) were obtained from two Tg rats. These cell lines had a polygonal cell morphology, expressed the typical choroid plexus epithelial cell marker, transthyretin, and possessed Na⁺, K⁺-ATPase on their apical side. TR-CSFBs cells expressed a large T-antigen and grew well at 33°C with a doubling-time of 3540 hr. [³H]-L-Proline uptake by TR-CSFB cells took place in an Na⁺-dependent, ouabain-sensitive, energy-dependent, and concentration-dependent manner. It was also inhibited by -methylaminoisobutylic acid, suggesting that system A for amino acids operates in TR-CSFB cells. When [³H]-L-proline uptake was measured using the Transwell device, the L-proline uptake rate following application to the apical side was fivefold greater than that following application to the basal side. In addition, both Na⁺-dependent and Na⁺-independent L-glutamic acid (L-Glu) uptake processes were present in TR-CSFB cells.Conclusions. Immortalized choroid plexus epithelial cell lines were successfully established from Tg rats and have the properties of choroid plexus epithelial cells, and amino acid transport activity was observed in vivo.     

Distinct role of adiposity and insulin resistance in glucose intolerance: studies in ventromedial hypothalamic-lesioned obese rats

It remains unclear whether adiposity plays an important role in glucose intolerance independently of insulin resistance. We investigated whether adiposity and insulin resistance had distinct roles in glucose intolerance in rats. We examined glucose tolerance and insulin resistance using ventromedial hypothalamic (VMH)-lesioned rats in the dynamic and the static phases of obesity (2 and 14 weeks after lesioning, respectively). Rats were fed either normal chow or a fructose-enriched diet (60% of total calories). The intravenous glucose tolerance test (IVGTT) was performed by bolus injection of glucose solution (1 g/kg) and blood sampling after 0, 5 10, 30, and 60 minutes. Insulin resistance was evaluated from the steady-state plasma glucose (SSPG) value during continuous infusion of glucose, insulin, and somatostatin. SSPG was not increased in VMH-lesioned rats in the dynamic phase of obesity, but increased markedly in the static phase. The area under the glucose curve (glucose AUC) during IVGTT was increased in VMH-lesioned rats in the static phase, but not in the dynamic phase, when compared with their sham-operated counterparts. A fructose-enriched diet for 2 or 14 weeks increased SSPG values to a similar extent in both sham-operated and VMH-lesioned rats without inducing excess adiposity, but glucose intolerance was only developed in the obese rats. The plasma leptin level, an excellent indicator of adiposity, was significantly related to the glucose AUC independently of the insulin level. Insulin resistance or increased adiposity alone is not sufficient to impair glucose tolerance, but increased adiposity plays an important role in the development of glucose intolerance in an insulin-resistant state.     

A 60-y-old chylomicronemia patient homozygous for missense mutation (G188E) in the lipoprotein lipase gene showed no accelerated atherosclerosis

BACKGROUND: Familial lipoprotein lipase (LPL) deficiency is a rare autosomal recessive disorder caused by mutations in the LPL gene. Patients with LPL deficiency have chylomicronemia; however, whether they develop accelerated atherosclerosis remains unclear. METHODS: We investigated clinical and mutational characteristics of a 60-y-old Japanese patient with chylomicronemia. RESULTS: The patient's fasting plasma triglyceride levels were >9.0 mmol/l. In postheparin plasma, one fifth of the normal LPL protein mass was present; however, LPL activity was undetectable. Molecular analysis of the LPL gene showed the patient to be a homozygote of missense mutation replacing glycine with glutamine at codon 188 (G188E), which had been known to produce mutant LPL protein lacking lipolytic activity. Ultrasonographic examination of the patient's carotid and femoral arteries showed no accelerated atherosclerosis. Moreover, 64-slice mechanical multidetector-row computer tomography (MDCT) angiography did not detect any accelerated atherosclerotic lesions in the patient's coronary arteries. The patient had none of the risk factors such as smoking, hypertension, and diabetes. CONCLUSIONS: Our case suggests that accelerated atherosclerosis may not develop in patients with LPL deficiency, when they have no risk factors.